I. Heart Failure--Need for Circulatory Assist
There is a need for medical equipment and methods for treatments that assist a beating heart of a patient suffering from heart disease or other weakened heart condition. When a heart becomes diseased or weak, the heart muscle deteriorates. The weakened heart muscle strains to pump sufficient amounts of blood through the patient's vascular system. The strain placed on the already-weak heart can lead to further deterioration and weakening of the heart. Treatments that assist a weakened heart to pump blood can be therapeutic by relieving some of the strain on a laboring, weakened heart.
The heart functions as two pumps in series. The right ventricle forces blood through the lungs into the left ventricle, and the left ventricle forces blood through the systemic circulation into the right ventricle. Small, but significant contributions to blood flow are also made by the skeletal muscle pump and the respiratory pump. In addition, the major periods of the cardiac cycle are diastole, during which the ventricles fill, and systole during which the ventricles eject blood.
To meet the demand for blood in a patient's vascular system, a weak heart increases its beat rate and devotes an increasing portion of its time and energy to pumping blood. The weak heart attempts to compensate for its weakness by working harder to pump blood through the vascular system. The straining heart diverts its time and energy away from sustaining itself with blood. In particular, the heart cuts short its rest stages during which blood normally flows into the heart muscle through the coronary arteries. When the rest stages become too short, the heart does not receive enough blood to sustain its already-weakened condition. By depriving itself of adequate amounts of blood, the heart contributes to its own deterioration. Accordingly, a weakened heart may deteriorate in a perilous cycle that increasingly strains the heart to pump blood and further reduces the blood supplied to the heart itself. This cycle can result in rapid heart deterioration (within a few hours or days) that leads to the irreversible failure of vital organs including the heart itself and possibly death.
A method to treat heart disease and other conditions in which a beating heart is weakened or over-strained is to assist the heart in pumping blood to the vascular system of the patient. By assisting the flow of blood, the strain (also referred to as load) on the heart can be artificially reduced.
The heart ejects blood from its left ventricular LV chamber into the aorta which leads to the vascular system. The "load" on the heart is the power required by the heart to eject blood from the LV chamber and aorta. Cardiac assist treatments reduce the load on the heart. When a weakened heart ejects blood against a reduced load, the heart can successfully evacuate more blood from the LV chamber and heart than would be evacuated without an assist volume. During each heart `stroke` the heart ejects more blood which leads to the increase of total blood flow, i.e., cardiac output, from the heart and through the vascular system.
In addition, by reducing some of the pumping load, the heart can devote more of its resources and time to providing blood to its own coronary arteries. Coronary arteries stem from the segment of the aorta that is closest to the heart and provide blood to the heart muscle. When the coronary arteries and muscle have sufficient blood flow, the heart has the ability to heal itself.
The heart often is prevented from healing itself when caught in the dangerous cycle of ever deteriorating and increasing strain. A cardiac assist treatment breaks this cycle by relieving the heart of some of its strain and reducing the load on the heart. Cardiac assist can treat a heart condition by relieving the load on the heart and allowing the heart to heal itself. Even if the heart is unable to heal itself, cardiac assist is beneficial because it prevents further deterioration and total heart failure, e.g., heart stoppage, until some other treatment, such as heart surgery, can be applied.
II. Existing Methods For Cardiac Assist
Ventricular Assistance has been attempted and, in some cases, accomplished by the following methods set forth in TABLE A:
TABLE A Intra-aortic balloon Pump (IABP) Heart bypass (Left Ventricular Assist Devices - LVAD and Right Ventricular Assist Devices RVAD) External upper body compression. Cardiopulmonary bypass also known as heart-lung machine Veno-arterial and Veno-venous bypass. External Leg Counterpulsation. Direct Mechanical Pressure on Heart.
Of all the methods listed in Table A, IABP is the method most commonly used as a clinical treatment. IABP counterpulsation is a method of providing temporary circulatory assistance to a failing and/or ischemic heart by providing reduced afterload and increased coronary perfusion pressure. In IABP, a balloon catheter is routed through the femoral artery, and positioned in the descending thoracic aorta with the tip of the catheter below the branches of the arteries that feed the heart (coronary) and brain (carotid).
The IABP device is synchronized with an ECG or arterial pulse tracing so that the balloon is rapidly inflated with an inert gas (helium) during the diastole phase of the heart cycle, and is rapidly deflated just before the onset of systole phase. The inflation of the balloon during diastole elevates the blood pressure in the aorta and drives blood into the heart muscle via the coronary arteries. As the balloon is rapidly deflated during systole, a low pressure zone is generated in the aorta. The aorta is, in effect, a large elastic vessel that stores a relatively-large volume of oxygenated arterial blood between heartbeats. The elastic aorta expands, during each heart cycle, to accommodate the added volume of blood called `stroke volume` ejected from the left ventricle and stored between heartbeats. The elasticity of the aorta resists expansion and, thus, the increased volume of blood pumped from the left ventricle. The resistance from the aorta is in proportion to the initial volume of the aorta, to which the `stroke volume` is added. The power applied by the left ventricle as it ejects blood is, in part, used to overcome the elastic resistance of the aorta and to push out the stroke volume of blood left in the aorta from the prior heartbeat cycle.
The balloon catheter used with IABP assists the heart by relieving the heart of some of the work of moving the stroke volume of blood out of the aorta to receive a new stroke volume. IABP displaces some of the volume of blood in the aorta by inflating the balloon with compressed gas to displace the stroke volume blood. By collapsing the balloon just before the left ventricle starts to eject blood, IABP creates a `void` in the aorta, which void is, at least partially, retained as a new stroke volume of blood is ejected from the left ventricle into the void left in the aorta. The void formed in the aorta by IABP reduces the tension of aortic walls and assists the left ventricle in its effort to eject blood by reducing the elastic resistance from the aorta to the stroke volume.
IABP has difficulty keeping up with the rapid heart rates associated with heart failure. When the cardiac cycle is shortened, the duration of diastole is reduced dramatically. The best modern IABP are believed to inflate the balloon in 120 ms minimum and deflate it in another 120 ms. These inflation and deflation rates are too slow to provide effective cardiac assist during each heartbeat cycle at high heart rates. IABP techniques may skip the inflation of the balloons during some heartbeats to facilitate synchronization with the heart cycle.
Other disadvantages of IABP balloon catheters are that they are invasive, require a surgical procedure for use and can be placed only by a specially trained interventional cardiologist, and can result in significant complications, such as amputation of the leg because the catheter prevents blood flow in the femoral artery.
A non-invasive cardiac assist alternative to IABP used in clinical practice is external leg counterpulsation. Examples of external leg counterpulsation are shown in U.S. Pat. Nos. 5,514,079, 5,218,954, 4,077,402 and 3,835,845; and EPO patent application No. 0 203 310 A2. Modern enhanced external counterpulsation involves the use of a device to inflate and deflate a series of compressive cuffs wrapped around a patient's calves, lower thighs, and upper thighs. Inflation and deflation of the cuffs are modulated by the cardiac cycle as monitored by computer-interpreted ECG signals.
During the diastole phase of the heart cycle, the cuffs inflate sequentially from the calves proximally, resulting in augmented diastolic central aortic pressure and increased coronary perfusion pressure. Rapid and simultaneous decompression of the cuffs at the onset of systole permits systolic unloading and decreased cardiac workload. The compression of the legs during heart diastole increases the coronary perfusion pressure gradient and coronary flow. The rapid decompression of the legs during systole reduces systolic arterial pressure which reduces the load on the heart.
The use of external leg counterpulsation is likely to encounter difficulties when used in acute heart patients or patients with severe heart failure. In response to the cardiogenic shock state that occurs during severe heart failure, the body initiates a number of compensatory mechanisms which seek to restore circulatory homeostasis. Skin, skeletal muscle, and kidney vascular beds undergo vasoconstriction to maintain mean arterial pressure and to preserve coronary and cerebral perfusion. Vasoconstriction reduces the blood flow through the legs and, thus, reduces the potential benefit achieved by the cuffs applied to the legs and other extremities in external counterpulsation treatments.
Moreover, an increase in sympathetic tone increases the heart rate and myocardial contractility, thereby maximizing cardiac output. It is highly unlikely that an external counterpulsation system can sequentially inflate and deflate a series of leg cuffs in the short cycle time of a rapid heartbeat. In addition, at high heart rates diastolic perfusion plays a lesser role and systolic perfusion (normally insignificant) starts to play a greater role in total coronary flow. Counterpulsation (by external leg compression or by intra-aortic balloon) can only increase coronary diastolic flow. Accordingly, counterpulsation does not assist with systolic perfusion.
In addition, current leg counterpulsation devices from CardioMedics and Vasomedical weigh approximately 250 lbs. and require 20 Amps AC current to operate. Placement of cuffs on the patient requires substantial time and equipment that may not be available during a heart failure emergency.
Another treatment for assisting a beating but weak heart is to externally compress a portion of the chest, thorax and/or abdomen of a patient's body. Examples of these external compression techniques are disclosed in U.S. Pat. Nos. 4,928,674, 4,971,042, 4,397,306, 5,020,516 and 5,490,820. The compression is applied to force blood out of the compressed region of the body and into other regions of the patient's vascular system. The external compression must be synchronized with the patient's beating heart, which is itself pumping blood, albeit at a reduced capacity and pressure. External compression treatment assists the heart by reducing the pumping load on the heart. When partially relieved of its load, the heart is able to increase the amount of blood ejected with each stroke and to allow blood to better circulate through its own muscle tissue between strokes.
There are some apparent advantages to cardiac assist by external compression relative to balloon catheters. For example, external compression does not require surgery and sterile conditions, as does IABP. External compression generally is not associated with risks of injury, and can be applied in emergency conditions, which often occur outside of a surgical room or intensive care units in the hospital. Despite these apparent advantages of external compression and the long-felt need for better cardiac assist treatments, there have been no successful cardiac assist treatments to humans using external compression.
Use of external chest compression during systole to unload the heart is counterintuitive. It is intuitive to apply counterpulsation to a patient's extremities to force blood towards a weakened heart without applying external compressive forces to the heart. In contrast to counterpulsation techniques, external chest compression applies pressure directly to the heart. One would expect that compression of the chest directly during systole would build up pressure inside the thorax (Intrathoracic Pressure--ITP) at the same time as the failing heart is struggling to eject blood into aorta. This rise of ITP would appear to be translated to the heart and aorta, and result in an increase in the systolic pressure that is commonly perceived as a measure of `afterload` that determines the work that the left ventricle has to perform to move blood. Accordingly, it would appear that external chest compression would increase the workload placed on a heart and would not provide any cardiac assist. However, this analysis does not take into account several factors including:
(a) The ITP does not primarily determine the workload on the heart. Rather, the wall tension of the heart muscle and the elastic resistance of the great thoracic vessels determines the workload of the heart. The internal resistance to coronary blood flow into the heart muscle is influenced by the volume of the distended heart and the blood pressure gradient across the heart wall (transmural pressure).
(b) When the thorax is compressed through external compression, the transmural pressure (Ptm) across the heart wall is the difference between intraventricular pressure (Plv) in the heart and the intrathoracic pressure (Ptm=Plv-ITP). The transmural pressure is indicative of the tension in the heart wall and, thus, indicates the workload on the heart. The transmural pressure is not determined by the difference between intraventricular pressure and atmospheric pressure.
(c) The heart is completely contained within the thoracic cavity and is approximately uniformly affected by the rise of ITP. Accordingly, increasing ITP does not produce blood pressure gradients within the heart. The aorta extends from the thorax and transverses the diaphragm. The aorta is only partially affected by the ITP change. Accordingly, blood in the aorta will be pushed across the diaphragm and into the abdomen when ITP increases.
(d) ITP is not uniformly distributed as a function of time and position inside the thorax, during the periods of chest compressions.
Under conditions of rapid chest compression and decompression at rates of 60 to 160 beats per minute (such as would occur in cardiac assist treatments), ITP `fluid pressure waves` are generated inside the chest cavity. These fluid pressure waves cause the distribution of intrathoracic pressure to vary across the inside of the chest cavity at any given time during the chest compression cycle. Animal research has indicated that during rapid chest compressions, the inertia of the abdomen (below the intrathoracic chest cavity) dominates the distribution of ITP inside the chest. Since abdominal motion lags considerably behind the chest wall motion, the ITP can be sub-atmospheric in some areas of the thorax while it is elevated to 20-25 mm Hg in others during each compression cycle. This mechanism is exploited by the current invention in a novel approach to create what can be called "hydraulic amplification" of a thoracic pump.
There is a need for an external chest compression system that is effective in unloading the heart of a patient suffering heart failure, and is synchronous with heart systole. Such a chest compression system would have considerable advantages over all (invasive or external) counterpulsation methods because: (a) external chest compression methods do not operate during diastole and therefore are not limited by the increase of the heart rate that often follows heart failure and tends to reduce the duration of diastole, and (b) these methods do not require prediction of the beginning of the next heart cycle time intervals (required for IABP or external leg counterpulsation) that is complicated by arrhythmia that is often associated with heart failure.
External chest compression methods have the potential of not only unloading the heart, but they have the capability of propelling blood forward out of the heart and adding external mechanical energy to the heart ejection process. In contrast, counterpulsation methods do not propel blood out of the heart and do not add energy to the heart. With counterpulsation methods, the useful work to move blood is performed by the heart itself.
Although at least some of the advantages of the chest compression method were known since the mid-1970s, prior attempts to develop a usable cardiac assist treatment using external compression of the upper body have not succeeded for a variety of reasons. The principal among these are believed to be:
(a) Difficulty of finding a method that will allow generation of substantial or `clinically significant` blood flow by applying pressure levels that the conscious patient can tolerate.
(b) Difficulty in synchronizing compressions with the beating heart, and in applying sufficient external pressure at the relatively rapid and variable cycle rates needed by a failing heart.
It was perceived by early developers that high pressures had to be applied to the chest to generate substantial blood flow. For example, U.S. Pat. No. 4,971,042 describes a cardiac assist cuirass that applies pressures as high as 250 mm Hg to the chest of a patient. In tests conducted by applicants, the application of as little as 70 mm Hg compression to the chest made the human volunteers very uncomfortable and caused substantial pain. In addition to high pressures, prior external thorax compression methods suffered from the notions that a cardiac assist treatment required: (a) simultaneous chest compression and lung ventilation, and/or (b) abdominal binding or compression of the abdomen in combination with chest compression. For example, U.S. Pat. No. 4,397,306 ('306) discloses an integrated system for cardiopulmonary resuscitation and circulation support which combines ventilation at high airway pressure simultaneous with chest compression. In addition, the system disclosed in the '306 patent tightly binds the abdomen to cause substantial amounts of abdominal pressure during chest compression, which is combined with negative diastolic airway pressure ventilation to move greater amounts of blood into the chest during diastole.
Ventilation of the lungs, which may in theory be useful, does not work well in practice. The difficulties encountered with lung ventilation include:
a) Inflating the lungs rapidly to substantial pressure levels required intubation that is a difficult and painful procedure.
b) When inflating lungs rapidly to substantial pressure levels fragile lung structures can be easily damaged.
c) While lungs can be inflated rapidly, it is practically impossible to deflate them equally rapidly without collapsing the airway. This led to dangerous `trapping` of the air in the lungs.
In addition, the inability of synchronized ventilation to follow high heart rates is described in U.S. Pat. No. 5,020,516.
Moreover, abdominal binding does not provide the expected amplification of ITP. Applicants, in connection with the present invention, recognized that abdominal binding does not increase the ITP. At the time of the invention, abdominal bindings were viewed as beneficial and it was not understood why they were counterproductive. Abdominal bindings appeared to be useful in restraining the abdomen to prevent the chest cavity from bulging into the abdomen while compressive forces were applied during chest compression. By restraining the abdomen and preventing bulging of the thorax, the increase in ITP would be elevated which should improve the cardiac assist treatment.
However, applicants found that while abdominal restraints did amplify the pressure in the chest, blood flow actually went down when using abdominal restraints. Prior to applicants' invention, Dr. Gruben speculated that during CPR at high compression rates, abdominal motion dominates the distribution of blood pressure in the chest. Dr. Gruben also discovered that when the abdomen was bound this phenomenon disappeared and the pressure distribution became uniform. However, Dr. Gruben had no means of measuring blood flow and never investigated the effects of unrestricted abdominal motion on blood flow.
An ineffective lung inflation plus abdominal binding approach is shown in U.S. Pat. No. 4,424,806, which discloses simultaneous lung inflation and abdominal compression. Another example of a prior cardiac assist treatment using "enhanced" external compression by a vest with inflatable bladders is shown in U.S. Pat. No. 5,490,820 ('820 patent). The '820 patent describes a vest assist device having multiple bladders arranged around the chest of a patient such that one set of bladders is positioned over the front of the chest, and other bladders are positioned at the sides of the chest. According to the system disclosed in the '820 patent, the bladder at the front of the chest (anterior bladder) is inflated when the ECG instrument monitoring the heartbeat detects the dicrotic notch in the arterial pressure waveform. The inflated anterior (front) bladder is supposed to flatten the chest and generate positive intrathoracic pressure--increase diastolic aortic, and, as a result, coronary perfusion pressure. The anterior bladder remains inflated until the onset of the systole portion of the heart cycle. At the onset of systole, the anterior bladder is deflated and the lateral (side) bladders are inflated to help restore the chest shape and generate negative intrathoracic pressure during systole--afterload reduction.
Inflatable vests have been unsuccessfully proposed for cardiac assist. Suggestions have been made that vests initially designed for cardiopulmonary resuscitation (CPR) could be adapted for vest assist. For example, U.S. Pat. No. 4,928,674 (the '674 patent) discloses a CPR vest that was a precursor to the present invention. The vest system disclosed in the '674 patent generates cyclic fluctuations in intrathoracic pressure primarily for CPR--not cardiac assist. However, the '674 patent makes a passing reference to cardiac vest assist by stating that vest inflation can be synchronized to an external signal, such as, a processed electrocardiograph, to assist a failing but still-beating heart.
Cardiac assist treatment is unlike (CPR). Cardiac assist treatment is done while the heart is still beating. The treatment assists the beating heart in moving blood through the vascular and coronary systems. CPR is done after the heart has failed and stopped beating. CPR (unlike cardiac assist) provides the sole pumping action for moving blood in the vascular system of a patient while the heart has stopped beating on its own.
Cardiac assist is technically more difficult than CPR because the cardiac assist must be synchronized with the beat of the heart. If not synchronized to the heart, cardiac assist would be counter-productive and potentially harmful to the patient. Since there is no heartbeat with CPR, there is no need to synchronize the chest compression done during CPR with a heartbeat. The problems associated with synchronizing with a heartbeat have been a particular problem associated with cardiac assist treatments.
Cardiac assist systems using inflatable vests that provided external compression were the subject of a limited number animal and human tests conducted at The Johns Hopkins University, Maryland, U.S.A. These experiments were successful in animals but, in general, not in humans. In 1988, Johns Hopkins University reported successful application of the vest in only two human patients over two years. The University attributed these failures to the inability of the equipment to: (a) support patients with heart rates greater that 75-80 beats-per-minute (bpm), and (b) difficulty synchronizing to the ECG signal when the vest was running. While improvements were made to the apparatus between 1989 and 1993, they did not remedy the reported problems. In 1992, Johns Hopkins' investigators reported that no new human patients were successfully supported by the new apparatus in spite of several generations of changes and multiple attempts.
Prior animal experiments using external compression to assist a beating heart were successful only because the natural ability of the animal's heart to pace itself was destroyed in these experimental preparations and an external electric pacing signal was used to stimulate heart contractions at a desired rate. The same signal used to stimulate the heart was used to trigger the assist apparatus in anticipation of heart contractions.
Prior to the present invention, there were no known methods or apparatuses that had been successfully used to provide cardiac assist for humans. In particular, prior to the present invention it is believed that there were no known:
a) Successful techniques for synchronizing a vest assist system to a beating heart in humans;
b) Vest assist systems that would substantially improve blood flow without exceeding tolerable force levels on the chest of a patient;
c) Vest assist systems that could achieve the objectives of sup-paragraphs (b) and (c) without artificially manipulating a patient's airway and using synchronized lung inflation therapy.
There was a long-felt need for a non-invasive therapy for providing cardiac assist. There are hundreds of thousands of patients suffering from heart failure in the United States each year. Many more patients are suffering from heart failure in other countries. The conventional treatment for heart failure is surgery, including insertion of an IABP catheter. A non-surgical approach to treating heart failure would be safer for the patients suffering from heart failure and less costly. Moreover, non-surgical treatments may be done outside of the intensive care units of hospitals, which are already over-crowded and extraordinarily expensive. A better treatment for heart failure would not require surgery or an intensive care unit of a hospital, but would still provide effective treatment and, hopefully, a cure for heart failure.